Many advances have been made in the management of ST elevation myocardial infarction (STEMI) over the past three decades.1 This is owed to insight into role that thrombus has in the obstruction of the infarct-related artery (IRA) and the subsequent cascade of the myocardial ischaemia, cell oedema and myocardial necrosis. The institution of reperfusion therapy has revolutionised the care of patients with STEMI decreasing morbidity and mortality.2–5 This therapy, whether it be pharmacologic in the case of fibrinolysis or mechanical in the case of percutaneous coronary intervention (PCI), aims at restoring patency of the IRA and ultimately tissue perfusion. However, even with modern primary PCI, distal embolisation of thrombus is common and about a third of patients have impaired microvascular perfusion despite TIMI 3 flow in infarct vessel.6 This article will review the importance of thrombus in STEMI and approaches to management: mechanical and pharmacologic.
The Importance of Thrombus in the Pathophysiology of ST Elevation Myocardial Infarction
Mechanism of Acute Coronary Syndrome in the Formation of Thrombus
The pathophysiology of acute coronary syndrome (ACS) is rupture or erosion of the fibrous cap overlying lipid rich plaques within the arterial tree.1 This event exposes pro-inflammatory substances, ultimately resulting in platelet aggregation and formation of obstructive thrombus.1,7 Angiographic evidence of thrombus formation can be seen in more than 90 % of patients who present with ST elevation myocardial infarction (STEMI).8 Plaque rupture usually produces combination of red (cross-linked fibrin and red blood cells) and white (platelet aggregates) thrombus.9 Reperfusion therapy has become the cornerstone in the treatment of STEMI.10–13 The basis of this strategy is to restore epicardial blood flow either by the fibrinolysis of thrombus or by mechanical displacement of thrombus in the case of percutaneous coronary intervention (PCI).
The Effectiveness of Reperfusion Therapy – Early Success in Thrombus Management
The effectiveness of thrombolytic therapy has been well demonstrated in the Second international study of infarct survival (ISIS-2) study. This landmark randomised trial of 17,187 patients compared streptokinase alone, aspirin alone, the combination of aspirin and streptokinase vs neither in patients with suspected acute myocardial infarction (AMI).2 ISIS-2 demonstrated that streptokinase reduced mortality by 25 % and the combination of aspirin and streptokinase reduced mortality by 39 per cent.2 However, one of the limitations of fibrinolytic therapy is that reperfusion of the infarct artery is only successful in 50–60 % of cases.14 In comparison, primary PCI achieves TIMI 3 flow in 80–90 % of cases and meta-analyses of randomised trials show that PPCI compared to fibrinolysis reduces mortality.5,15